Osthole ameliorates myonecrosis caused by Clostridium perfringens type A infection in mice

作     者：Xueyong Zhang Yue Liu Zhangqi Shen Shaolin Wang Congming Wu Dejun Liu Shusheng Tang Chongshan Dai 

作者机构：National Key Laboratory of Veterinary Public Health and SafetyCollege of Veterinary MedicineChina Agricultural UniversityBeijing 100193China Guangdong Laboratory for Lingnan Modern AgricultureGuangzhou 510642China 

出 版 物：《One Health Advances》 (全健康进展（英文）)

年 卷 期：2023年第1卷第1期

页      面：52-61页

学科分类：1008[医学-中药学(可授医学、理学学位)] 1006[医学-中西医结合] 100602[医学-中西医结合临床] 10[医学] 

基　　金：funded by Laboratory of Lingnan Modern Agriculture Project(Award number NT2021006) supported by the National Natural Science Foundation of China(Award number 32102724) Pinduoduo-China Agricultural University Research Fund(No.PC2023A01002) 

主　　题：C.perfringens Myonecrosis Osthole Nrf2/HO-1 pathway NF-κB pathway 

摘      要：This study aimed to investigate the protective effect of the nature product osthole(OST)against Clostridium perfrin-gens type A infection-caused myonecrosis in a mouse *** mice were divided into(1)control,(2)infected,(3)OST50 and(4)OST100 treatment *** the infected groups,mice were intramuscularly injected with 1×10^(8) CFU of *** per day for 6 *** in the OST50 and OST100 groups were administrated intraperitoneally with OST at the doses of 50 or 100 mg/kg per day post *** *** results showed that *** infection caused marked necrosis and inflammatory cell infiltration in the muscle tissues of *** in the OST50 and OST100 treatment groups displayed significantly attenuated *** infection-induced lipid peroxida-tion,oxidative stress,and apoptosis in their muscle ***,OST treatment significantly downregulated the expressions of NF-κB,IL-1β,and TNF-αmRNA and protein levels,while concomitantly upregulating the expressions of Nrf2 and HO-1 mRNA and *** treatments also inhibited the expression of phosphorylation(p)-p38,p-mTOR,and p-Erk1/2 proteins,and upregulated LC3II and Beclin1 *** summary,our results reveal that OST therapy confers a protective effect against *** infection-induced oxidative stress and inflammation in muscle tissue,via activation of Nrf2/HO-1 and autophagy pathways and inhibition of p38,Erk1/2 and NF-κB pathways.